Community pharmacy is the key to improving vitamin D levels.

Introduction: Vitamin D is an essential micronutrient that participates in the body's fundamental physiological processes. The pharmacist should involve the patient in his medication adherence, leading to a change in the patient's attitude towards his medication and towards his health problem, in order to achieve the pharmacological objective set. Methods: Quasi-experimental multicenter study design with non-probabilistic convenience sampling. A pharmacist-led intervention in health education was carried out, divided in two groups, face-to-face interview and on-line survey, and the results were evaluated 3 months later to observe if there was any change in the patient's health status or in their vitamin D levels. Results: The study was conducted in four pharmacies through face-to-face interviews (n = 49 patients) and online surveys (n = 23). Pharmaceutical intervention improved habits of exercise (0.81 ± 1.44 days/week face-to-face interviews vs -0.09 ± 2.35 days/week online surveys (p = 0.048)). In face-to-face interviews, consumption of vitamin D-rich foods was increased (0.55 unit of tuna/week; p = 0.035 and 0.56 unit of avocado/week; p = 0.001) and was improved correct intake of vitamin D supplements (32.5% baseline to 69.8% at 3 months). The increase in 25-hydroxyvitamin D levels (11.5 ng/mL after 3 months (p = 0.021)) was correlated to salmon consumption (0.951; p = 0.013) and the improvement of quality of life was correlated to avocado consumption (1; p < 0.001). Conclusion: There are habits that improve vitamin D production such as increased physical activity, the correct use of vitamin D supplements and the consumption of foods with high vitamin D levels. The role of the pharmacist is crucial, involving the patient in the treatment making aware of the benefits for his/her health status of increasing vitamin D levels.

PPARß activation restores the high glucose-induced impairment of insulin signalling in endothelial cells.

BACKGROUND AND PURPOSE: PPARß enhances insulin sensitivity in adipocytes and skeletal muscle cells, but its effects on insulin signalling in endothelial cells are not known. We analysed the effects of the PPARß/δ (PPARß) agonists, GW0742 and L165041, on impaired insulin signalling induced by high glucose in HUVECs and aortic and mesenteric arteries from diabetic rats. EXPERIMENTAL APPROACH: Insulin-stimulated NO production, Akt-Ser(473) and eNOS-Ser(1177) phosphorylation, and reactive oxygen species (ROS) production were studied in HUVECs incubated in low- or high-glucose medium. Insulin-stimulated relaxations and protein phosphorylation in vessels from streptozotocin (STZ)-induced diabetic rats were also analysed. KEY RESULTS: HUVECs incubated in high-glucose medium showed a significant reduction in insulin-stimulated production of NO. High glucose also reduced insulin-induced Akt-Ser(473) and eNOS-Ser(1177) phosphorylation, increased IRS-1-Ser(636) and ERK1/2-Thr(183) -Tyr(185) phosphorylation and increased ROS production. The co-incubation with the PPARß agonists GW0742 or L165041 prevented all these effects induced by high glucose. In turn, the effects induced by the agonists were suppressed when HUVEC were also incubated with the PPARß antagonist GSK0660, the pyruvate dehydrogenase kinase (PDK)4 inhibitor dichloroacetate or after knockdown of both PPARß and PDK4 with siRNA. The ERK1/2 inhibitor PD98059, ROS scavenger catalase, inhibitor of complex II thenoyltrifluoroacetone or uncoupler of oxidative phosphorylation, carbonyl cyanide m-chlorophenylhydrazone, also prevented glucose-induced insulin resistance. In STZ diabetic rats, oral GW0742 also improved insulin signalling and the impaired NO-mediated vascular relaxation. CONCLUSION AND IMPLICATIONS: PPARß activation in vitro and in vivo restores the endothelial function, preserving the insulin-Akt-eNOS pathway impaired by high glucose, at least in part, through PDK4 activation.

Different cardiovascular protective effects of quercetin administered orally or intraperitoneally in spontaneously hypertensive rats.

We tested whether the administration procedure of quercetin affects its metabolite profile and antihypertensive activity. Spontaneously hypertensive rats (SHR) were randomly assigned to four experimental treatments: (1) 1 mL of 1% methylcellulose by oral gavage and 2% DMSO i.p. (control group); (2) 10 mg kg⁻¹ quercetin by oral gavage once daily and 2% DMSO i.p.; (3) 10 mg kg⁻¹ quercetin by oral gavage divided in two daily doses (5 + 5 at 12 h intervals) and 2% DMSO i.p.; (4) 1 mL of 1% methylcellulose by oral gavage and 10 mg kg⁻¹ quercetin i.p. injection. Rats were treated daily for 5 weeks. Single dose and two daily doses, in a long-term oral treatment were equally efficient, both restoring the impaired aortic endothelium-dependent vasodilatation and reducing mesenteric contractile response to phenylephrine, systolic blood pressure, heart rate, and heart and kidney hypertrophy. Attenuation of vascular NADPH oxidase-driven O2⁻ production was also found in orally treated rats. Intraperitoneal administration reduced, to lesser extent than oral administration, the increased systolic blood pressure, being without effect to the endothelial dysfunction and vascular oxidative stress. In contrast, greater levels of metabolites were quantified following intraperitoneal compared to oral administration at any time point, except for higher plasma methylated quercetin aglycone in oral as compared to intraperitoneal administration at 2 but not at 8 h. In conclusion, oral quercetin was superior to intraperitoneal administration for the protection from cardiovascular complications in SHR. No differences were found between the oral administration as a single daily dose or divided into two daily doses.